Talk:Senescence

From Wikipedia, the free encyclopedia

WikiProject Biology
Biology Portal

Senescence is part of the WikiProject Biology, an effort to build a comprehensive and detailed guide to biology on Wikipedia.
Start This article has been rated as start-Class on the quality scale. See comments.
Mid This article has been rated as mid-importance on the importance scale.
To-do list for Senescence: edit · history · watch · refresh
Priority 3  

Contents

[edit] Simple species that do not age

I have read somewhere that some worms (like tapeworm) never get old and all of their cells keep dividing without limit. Where can I find scientific references about it?

[edit] Senescence manifests

Althought It might seem stupid to ask it's not, what is characteristic of senescence? I mean, anyone knows senescent people have wrinkles... But... Ia that all? I mean, are there any other indications of old age? Most people see the wrinkles and make the decision, if they do not see wrinkles then there is no old age... But this... It's not accurate... There are more... Mmmm... To say so "symptoms" of old age... Aren't they? _____________

Theories of aging taken from http://jap.physiology.org/cgi/content/full/95/4/1706

Biological Level/Theory -- Description

Evolutionary

  • Mutation accumulation -- Mutations that affect health at older ages are not selected against.
  • Disposable soma -- Somatic cells are maintained only to ensure continued reproductive success; after reproduction, soma becomes disposable.
  • Antagonistic pleiotropy -- Genes beneficial at younger age become deleterious at older ages.

Molecular

  • Gene regulation -- Aging is caused by changes in the expression of genes regulating both development and aging.
  • Codon restriction -- Fidelity/accuracy of mRNA translation is impaired due to inability to decode codons in mRNA.
  • Error catastrophe -- Decline in fidelity of gene expression with aging results in increased fraction of abnormal proteins.
  • Somatic mutation -- Molecular damage accumulates, primarily to DNA/genetic material.
  • Dysdifferentiation -- Gradual accumulation of random molecular damage impairs regulation of gene expression.

Cellular

  • Cellular senescence-Telomere theory -- Phenotypes of aging are caused by an increase in frequency of senescent cells. Senescence may result from telomere loss (replicative senescence) or cell stress (cellular senescence).
  • Free radical -- Oxidative metabolism produces highly reactive free radicals that subsequently damage lipids, protein and DNA.
  • Wear-and-tear -- Accumulation of normal injury.
  • Apoptosis -- Programmed cell death from genetic events or genome crisis.

System

  • Neuroendocrine -- Alterations in neuroendocrine control of homeostasis results in aging-related physiological changes.
  • Immunologic -- Decline of immune function with aging results in decreased incidence of infectious diseases but increased incidence of autoimmunity.
  • Rate-of-living -- Assumes a fixed amount of metabolic potential for every living organism (live fast, die young).

Shouldn't this be at Ageing? (currenty a redirect) That is by far the more common name. - SimonP 17:10, Jun 11, 2004 (UTC)

Ageing is spelled aging in the US. Let's keep it senescence. Speciate 07:31, 13 January 2007 (UTC)

I watched a show on the Science Channel on TV. It mentioned that scientists had observed that ageing stops after age 95. Theoretically if they can find out how it is switched off at age 95, then they can find a way to switch it off at an earlier age, such as at a man's prime. Is this claim true? Can someone research it deeper and add the findings in the article. Kowloonese 10:54, 12 Nov 2004 (UTC)

[edit] Link between stress and aging

Should this study be noted in the biological causes, or should we wait for confirmation? (Obviously it is required, eventually.) —Daelin 04:15, 30 Nov 2004 (UTC)

[edit] The text below should be merged with the article

  1. Careful studies of health statistics support a systems approach to aging. When enough systems are damaged, a catastrophic failure occurs.
  2. Dr. Leonard Hayflick discovered that mammalian cells divide only a fixed number of times. This "Hayflick limit" was later proven to be caused by telomeres on the ends of chromosomes that shorten with each cell-division. When the telomeres are gone, the DNA can no longer be copied, and cell division ceases. In 2001, experimenters at Geron Corp. lengthened the telomeres of senescent mammalian cells by introducing telomerase to them. They then became youthful cells. Sex and some stem cells regenerate the telomeres by two mechanisms: Telomerase, and alternative lengthening of telomeres (ALT). At least one form of progeria (atypical accelerated aging) is caused by premature telomeric shortening. Also in 2001, research showed that naturally occurring stem cells must sometimes extend their telomeres, because some stem cells in middle-aged humans had anomalously long telomeres.
  3. Experimenters discovered that mice whose pituitary glands were removed lived half again as long as unmodified mice, though with terrible side-effects. Therefore, mammals are believed to have a hormonal system that triggers some age-related disease. However, humans with their pituitary glands removed do not live longer.
  4. In 2002, genetic modification of a small worm (Caenorhabditis elegans) increased its lifespan sixfold. Related experiments have increased maximum life-span in mice and fruit flies. These experiments prove that there is a genetically-coded death clock that triggers some part of aging. This may be related to the hormonal death clock.
  5. A number of research programs have proven that mutations in body cells occur and accumulate as an organism ages, and degrade its function. In 1999, researchers discovered that naturally occurring stem cells recolonize organ systems, countering this effect by reintroducing cells from a reduced number of cellular lineages. The number of cellular lineages is further decreased because the older half of the reproduced DNA is far more likely to remain in a stem cell. The mechanism of old-strand conservation is still being researched.
  6. A number of clinicians noted that the cumulative damage in diabetic patients strongly resembled accelerated aging. This was generalized into a theory that some aging is caused when sugar chemically combines with proteins and other bodily chemicals. It is known that feeding adolescent mice a fully-nutritive diet with minimal food energy can extend their maximum life-spans by half. It is also known that feeding mice small amounts of chromium picolinate can extend their maximum life span about 15%. Chromium is an integral part of active insulin, and insulin is cleaved, to excrete chromium in normal metabolism. Most adult nonvegetarians have large amounts of inactive insulin, which may indicate a chronic deficiency of dietary chromium. Veterinarians routinely treat middle-aged animals for diabetes with chromium supplementation.
  7. Studies of patients with Alzheimer's disease patients and age-spotting discovered that the body builds deposits of waste within and without cells. The deposits inside cells are called lipofuscin (Latin for "fat dirt"). These deposits may decrease metabolic efficiencies, causing some age-related symptoms. Mammalian cells have enzymes to cleave and digest proteins. The most common such clean-up enzyme is triggered by a three-element chain of Ubiquinone (CoQ10) attached to the elderly protein.
  8. Dr. Denham Harman theorized that some aging damage might be caused by oxidative damage to the body. Experiments discovered that the body has substantial amounts of enzymes and chemicals to reverse oxidative changes. Studies also showed that longer-lived animals have larger amounts, per weight of animal of these mechanisms, in a linear relation to life-span. The experiments also found an internal mechanism, respiration in mitochondria, that creates free radicals that would cause oxidative damage. Feeding of antioxidants to mice increased average life-spans, but not maximum life spans. It is now believed that oxidative damage depletes self-repair mechanisms, whose limits are controlled by other systems.
  9. The failures of natural stem cells are now an active area of research. In many cases of damaged organ systems, stem cells do not migrate to the damaged area.
  10. Experimenters discovered that mice fed extra melatonin lived 20 percent longer than control mice.


[edit] BEFORE YOU ADD TO THIS ARTICLE....

...read WP:AWW. This article presents a myriad of scientific theories and hardly cites any of them. Most theories are preceded by "some gerontologists blieve" or "research has shown" .....you get the idea. These forms of claims are unreputable and require citations. There is a ton of good information in this article, but it needs to be appropriately cited.

If you have the information to add, it shouldn't be that much trouble to cite it. And remember, citing it does not just (or even necessarily) mean putting the title of a book at the bottom of the page. In-line citations are great, and describing the history of a development of a theory adds legitimacy as well.

Keep up the good work guys, and keep being bold. Just remember to cite as you go. Shaggorama 05:45, 27 April 2006 (UTC)

[edit] Proposed merge

Also see discussion here. - Samsara (talk • contribs) 14:41, 13 June 2006 (UTC)

[edit] Propose renaming to biology of ageing

While I acknowledge that senescence is a term typically applied to a wider range of taxa than "ageing" (e.g. plants typically "senesce" rather than "age"), I think the article would become more approachable (yes, because the links would be labelled with something intelligible for the average Joe) by renaming it to "biology of ageing". - Samsara (talk • contribs) 14:45, 13 June 2006 (UTC)

There is always #redirect for the average Joe. Encyclopedia should use more formal terminologies instead of everyday English. Kowloonese 17:12, 13 June 2006 (UTC)
Well, that's exactly my point. "Biology of ageing" in my experience is more commonly used to refer to the study of senescence in humans, which presumably is of interest to most people coming to read this kind of article; secondly, it would much simplify what's being done here. Just because it's latinised doesn't mean it's right. The best books in science were written in prose that a layperson could follow. - Samsara (talk • contribs) 17:22, 13 June 2006 (UTC)

Ageing is spelled aging in the US. Let's keep it senescence Speciate 07:28, 13 January 2007 (UTC)

[edit] Merging Aging DNA into this article and/or mentioning it

The article on Aging DNA seems to be a bit orphaned, but it merits some mention, if not inclusion, in both this article and the one on DNA repair. IMHO, it should remain its own article, and we could have this article make a mention of it in one or two paragraphs. However, I am not a professional geneticist, so I would like the input of some experts on where this should be mentioned/merged. The ikiroid (talk·desk·Advise me) 15:56, 4 August 2006 (UTC)

[edit] PNC1 is a Nicotinamidase, PBEF is NOT a Nicotinamidase

The protein PNC1 has been shown to play a key role in yeast aging. Mammals do not have a PNC1 homolog. Instead, we use a Nicotinamide phosphoribosyltransferase (Nampt or PBEF or visfatin, same protein, different names) enzyme to recycle NAD from nicotinamide. Even though they both play functional similar roles, they are, in fact, different enzymes, and it is therefore improper to call Nampt/PBEF/visfatin a nicotinamidase.

[edit] Re: Evolutionary theories

Why do not man live longer than women since they can reproduce up to a very old age and women cannot leading to a higher selection. —The preceding unsigned comment was added by 128.197.42.60 (talk) 22:10, 25 January 2007 (UTC).

Evolutionary theory is a bit more complicated than that; specifically, when determining whether a particular trait would have been subject to evolutionary selection, it is important to keep in mind the historical context of that trait. For the vast majority of human history, an individual's lifespan was on the order of 30 years. Disease, predators, and harsh living conditions prevented most individuals from reaching their maximum reproductive age, thus there was little evolutionary pressure for selecting individuals that could reproduce for the longest time. This is a specific case of the general maxim "the force of natural selection declines with age".

[edit] de Grey and SENS

I recently read the book "Ending Aging" by Aubrey de Grey about his Engineered negligible senescence. There is a lot of historic (and thus outdated) information in this article and the structure of it also conforms to older theories. While I am not sure how objective de Grey's book is, I am quite sure that a complete overhaul of the article would be a good thing to point out the currently leading theories. --84.178.118.140 13:34, 13 October 2007 (UTC)

[edit] Just to blow the telomerase dreamers' bubble, ...

... I added a long-overdue mention of the fact that cancers are immortals. Yes, (parts of) humans can become immortal!. In fact, there are probably a few cells in your body that are acquiring this ghastly property right now. You and I hope they will remain few.

All available science points to the fact that, if some crazy scientist can reactivate your telomerases at age 60, you will not have enough time to see your new youth before your body fills with tumors. Your life will thus be shortened, not lengthened, and you will die with the excruciating pain of bone metastases.

Pop goes the bubble. Emmanuelm (talk) 21:47, 19 November 2007 (UTC)

The majority of cancers, but not all, express telomerase. On the other hand, all embryonic stem cells express telomerase, and some other cells in the human body do, as well, e.g., some keratinocytes. Just as "inhibiting telomerase = curing cancer" is too simplistic, "activating telomerase = causing cancer" is, as well. --SierraSciSPA (talk) 18:08, 23 January 2008 (UTC)

[edit] Sources

If I've read the links correctly on my personal discussion page, things have to be sourced and neutral.

To quote: "The above categorisation of theories of aging is generally considered obsolete by biogerontologists.[citation needed]"

End quote.

If the statement is included, it looks like it would need multiple reliable citations. Otherwise, it is opinion, stated as fact. I looked for a reference, but could not find one. If you reinsert it, can you add the sources? WordMachine (talk) 13:10, 23 January 2008 (UTC)

I'll look for a source. In the meantime, you might want to reconsider trying to link the two paragraphs together with a simple "conversely," since its meaning is not very clear at all. Information does have to be sourced on Wikipedia, but I notice that the programmed and stochastic theories of aging are presented without any source whatsoever to indicate that they have scientific merit, or even that they were considered to have had scientific merit in the past. I'll try to get an expert opinion on this. --SierraSciSPA (talk) 18:18, 23 January 2008 (UTC)

[edit] Red Links (Wikipedians don't know bout this article's useless links)

If a link goes nowhere (commonly called by us trolls as "that red word"), please delink it. Or unlink it. Or non-link-ify it. Or some other of your high-learning vocab that means "Clean up this article." SgtHydra 71.111.76.124 (talk) 03:03, 26 January 2008 (UTC)

Red links are often considered useful reminders that an article on the subject should exist, and somebody needs to write it. I agree, though, that this article needs cleanup - certainly, no phrase needs to be red-linked more than once. --SierraSciSPA (talk) 00:07, 28 January 2008 (UTC)